Today, we discussed a case of diabetic ketoacidosis (DKA) in a patient with a new diagnosis of diabetes. DKA is characterized by an absolute or relative deficiency of insulin in which ketone acids accumulate in blood so as to cause a fall in arterial pH to less than 7.25 or a decrease in serum bicarbonate to less than 10 mEq per liter (or both).

It is always important to think about what the precipitant is for DKA, so here is a little mnemonic to help you remember the eight major causes that all start with the letter I:

Infection (think UTI, pneumonia, strep throat)

Inflammation (like pancreatitis)

Initial diagnosis

Infarction or ischemia (like an MI or stroke)

Insulin deficiency (patient not taking at all, not taking enough for their physiologic needs)

Infant (pregnancy)

Illegal drugs (cocaine, meth, etc)

Iatrogenic (mainly drug interactions, such as starting prednisone)

The cornerstones of management are:

1) Rapid intravascular volume repletion with IVF

Start with normal saline bolus, then continue at ~20mL/kg/hr

Switch to half isotonic saline if the *corrected* sodium is normal or elevated (corrected= for every 100 above normal glucose, add ~2 mEq of Na to the serum sodium level)

Add dextrose (can do D5 half NS) once the serum glucose is less than 200

2) Correction of hyperglycemia and acidosis with insulin drip. Only start if the K is > 3.3, otherwise replete first. The standard is an insulin drip often with 0.1 units/kg IV bolus, then start a continuous IV infusion 0.1 units/kg per hour. Stop the drip when: the patient's anion gap is closed, the patient is eating, and 1-2 hours after you have given SC insulin.

3) Electrolyte replacement as needed, particularly potassium. That is, regardless of the initial measured serum potassium, patients with DKA have a large total body potassium deficit.